Respiratory Failure

Medicine 2 Noel V. Bautista December 20, 2007

Causes of Respiratory Failure Organ/System Central Nervous System Peripheral Nervous System Neuromuscular System Examples Stroke, Drug overdose, Trauma, Myxedema Guillain-Barre syndrome, Spinal cord compression, Poliomyelitis Myasthenia gravis, Tetanus, Hypokalemic paralysis, Multiple sclerosis, Botulism, Organophosphate poisoning, Antibiotics (Kanamycin, Polymyxin), Curariform drugs Severe kyphoscoliosis, Flail chest, Massive pneumothorax or pleural effusion Epiglotitis, Tracheobronchitis, Vocal cord paralysis Pneumonia, COPD, Asthma, ARDS

Respiration - The exchange of gases between the organism and the environment Remember that respiration not only involved the lungs but all the organs Respiratory Failure - Respiratory failure is a condition in which the respiratory system is unable to perform its gas-exchange function i.e. oxygenation and/or carbon dioxide elimination Extended Concept of Respiration

Thorax and Pleura Upper Airway

Lower Airway and Alveoli Cardiovascular Heart failure System Blood Anemia, Polycythemia Cell/Tissue Sepsis, Cyanide poisoning We could therefore investigate causes of respiratory failure according to the structures involved in respiration Hemoglobin carries 98% of oxygen to be delivered to body cells Types of Respiratory Failure Type 1 (Normocapnic Respiratory Failure) Hypoxemia with eucapnia or hypocapnia - Pure oxygen problem Type 2 (Hypercapnic Respiratory Failure) Hypoxemia with hypercapnia - Oxygenation and ventilation (e.g. involving CO2) problem

The respiratory system is a pump that facilitates gas exchange main function: maintain metabolic function - Ventilation and perfusion of organs should be properly matched for ideal oxygenation of blood which delivers oxygen to individual organ systems to maintain optimum metabolic activity and homeostasis - Oxygen is important in aerobic glycolysation - Carbon dioxide should also be effectively eliminiated or would lead to acidosis External Respiration exchange of gas between environment and respiratory system Internal Respiration exchange of gas at cellular level Cellular metabolism driving force of ventilation Better Definition of Respiratory Failure - Respiratory failure is present when the pulmonary system is unable to meet the metabolic demands of the body Respiratory Failure

Respiratory Failure

Hypoxemia

Hypercapnia

Oxygenation Failure

Ventilatory Failure

Respiratory System Disorders Aiways Lungs

Ventilatory Pump Disorders Nervous System Thorax Respiratory Muscles Respiratory System

Acute

Acute

Develops over several hours or longer Kidneys compensate for the respiratory acidosis Classification of acute and chronic is very arbitrary there is no defining line Acute respiratory failure subcellular level has not yet been able to adapt to the disturbance Major adaptation in gas exchange is achieved by kidneys however before the kidney participates, a buffer system first tries to compensate Chronic respiratory failure kidneys have already adapted; kidney adaptation could happen in a matter of hours or days which is why classification into acute or chronic is arbitrary Develops in Minutes to a few hours

RF will always produce acidosis. Thus it is important to know oxygenation status (by looking at ABG) and ventilation status (by looking at CO2 status) - ABG involves - Oxygenation status - Ventilatory status - Acid-base disturbance Ventilation failure usually involves CNS, thorax, respiratory muscles; most of time lungs not affected. Oxygenation failure usually parenchyma of lungs Ventilation and PaCO2 Ficke equation: PaCo2 = VCO2 x 0.863 VA PaCO2 ~ VA - the lower the ventilation, the more CO2 accumulates VE = V A + V D VE = V T x f VA = (VT x f) VD VE minute ventilation VA alveolar ventilation VD dead space ventilation VT tidal volume f respiratory rate

CO2 elimination is usually 250 mL/min How do get an idea of the status of alveolar ventilation: check PaCO2 1

Minute ventilation affected by: Tidal volume, respiratory rate, and dead space ventilation Respiratory rate (tachypneic) does not assure you adequacy of ventilation Ventilatory Pump Failure - Central nervous system - Peripheral nervous system - Thorax & Pleura - Respiratory muscles myasthenia gravis Hypercapnia results from disturbance in ventilatory pump Causes of Hypoventilation (Hypercapnia) - Brainstem - brainstem injury due to trauma, hemorrhage, infarction, hypoxia, infection etc - metabolic encephalopathy - depressant drugs - Spinal cord - trauma, tumor, transverse myelitis - Nerve root injury - Nerve - trauma - neuropathy eg Guillain Barre - motor neuron disease - Neuromuscular junction - myasthenia gravis - neuromuscular blockers - Respiratory muscles - fatigue - disuse atrophy - myopathy - malnutrition - Respiratory system - airway obstruction (upper or lower) - decreased lung, pleural or chest wall compliance Causes of Ventilatory Failure Fever, hypermetabolism Lung parenchyma disorders e.g. COPD, asthma, ARDS, pulmonary embolism Decreased ventilatory drive e.g. sedation or Pump failure e.g. neuromuscular disease If blood gases reveal hypercapnea, try to categorize them into the above three pathophysiological processes: 1. Increased CO2 production; rarely the cause, but can be an additional factor that adds to hypercapnea More important factor is still diminished alveolar ventilation, not increase CO2 production so can forget about this, usually it is only co-conspirator however by itself will not cause hypercapnia 2. Increase in dead space (Minute ventilation is sum of alveolar ventilation and dead space ventilation) which will decrease alveolar ventilation. CO2 accumulates. Seen in obstructive airway diseases 3. Decreased alveolar ventilation Respiratory System Oxygenation - Inspired gases (PiO2, PiCO2) - Alveolar ventilation (Va, PAO2, PACO2) - Diffusion of gas through the respiratory membrane (DmO2) - Perfusion of pulmonary capillaries - Ventilation-perfusion matching (V/Q) Whenever there is hypercapnea, find reason. Do not rely on respiratory rate request for PaCO2 oxygenation failure so many causes Inspired Air
Inspired Air: dry O2 160 mmHg (21%) N2 600 mmHg (79%) CO2 0 mmHg (0%) H2O 0 mmHg (0%)

Daltons Law: PB (barometric pressure) = PN2 + PO2 + PCO2 + PH2O = 760 mmHg (at sea level) normal atmospheric pressure Barometric pressure is the sum of all the partial pressures of the most important gases in atmosphere Nitrogen is an inert gas; we breathe it without any physiological consequence Gas that we inhale is humidified PiO2 = FiO2 x PB FiO2 = PiO2/PB = 160/760 = 21% PiO2 fraction contributed by O2 FiO2 available oxygen Effects of Altitude on Barometric Pressure Altitude (Feet) PB (mmHg) PiO2 (mmHg) 0 760 159 10,000 523 110 20,000 349 73 30,000 226 47 40,000 141 29 50,000 87 18 In the urban setting, decreased FiO2 is rarely the reason for respiratory failure, except in cases of fire, CO poisoning Alveolar Gases - amount O2 that reaches alveoli

Increased VCO2 Increased VD and Decreased VA Decreased VA

Alveolar Air Saturated O2 100 mmHg (13%) N2 573mmHg (76%) CO2 5mmHg (40%) H2O 47mmHg (6%)

Alveolar air equation: PAO2 = (PB PH2O) x FiO2 (PaCO2/RQ) = (760 47) x FiO2 (PaCO2/RQ) = 713 x FiO2 (PaCO2/RQ) = 713 x 0.21 (40/0.8) = 99.7 mmHg Alveolar Capillary Membrane - When O2 reaches alveoli, next step is perfusion - Ficks law: involves diffusion of gas on surface

Tracheal Air: Saturated O2 150 mmHg (20%) N2 563 mmHg (74%) CO2 0 mmHg (0%) H2O 47 mmHg (6%)

Ficks Law of Diffusion: VO2 = DmO2 x ( PAO2 PCO2) Dm = Diffusing Capacity (Note: D is directly proportional to Area and Diffusion Coefficient for the gas and inversely proportional to diffusion Distance ~ D = [A x Dc]/T) *No need to memorize or apply equation what is important is that alveolar membrane should be in tip-top shape for the respiratory gases to diffuse through Diffusion is fast takes only a quarter of a second for desaturated gas to be completely oxygenated So even if you exercise diffusion or the respiratory system is usually not the problem but the cardiovascular system Exercise can improve the cardiovascular system improve oxygen delivery from 10-15x, but the reserve capacity of the cardiovascular system is even more (20-25x) in a normal resting physiologic bodies Bottomline: Diffusion is not a usual cause of hypoxemia 2

Ventilation-Perfusion Matching - The usual cause of hypoxemia

Effect of Hypoventilation on Hypoxemia Va PAO2 PaO2 Va PaCO2 PaO2 1mmHg ~ 1.25mmHg Fixed Variable PB = PN2 + PH2O + PCO2 + PO2 760 573 47 40 100 mmHg
Low V/Q Ventilation Shunt

Dead space Ventilation

High V/Q Ventilation

Normal V/Q ratio = 0.8 VQ matching or mismatching comes in a spectrum of physiologic events A complete ventilation but no perfusion; physiologic dead space B ideal VQ; ventilation is matched by perfusion. Normal VQ slightly more perfusion than ventilation; some of blood flow goes back to heart unoxygenated. D no ventialtion but complete perfusion; shunt Hard to determine A and D from one another; often lumped together Alveolar-Arterial Oxygen Gradient

Example: PaCO2 = 55 mmHg (change = 55 40 = 15) Expected PaO2 = 80 mmHg (80 15 x 1.25) = 61.25 If actual < expected hypoventilation (plus other) Hypoventilation Actual PaO2 = 60 mmHg Ventilation-Perfusion Mismatching - Causes: - Airway disorders - Lung parenchymal disorders Most common cause of V/Q mismatch: Obstructive airway disease Shunt Defect Shunt Equation: Qs = CcO2 CaO2 = 5-8% QT CcO2 CvO2 Causes: - Intracardiac - Right to left shunt e.g. Fallot's tetralogy, Eisenmenger's syndrome - Pulmonary - Pneumonia - Pulmonary edema - Atelectasis - Pulmonary haemorrhage - Pulmonary contusion Dead Space Ventilation
Ventilation

PAO2 = 100 115 mmHg P(A-a)O2 = 15=20 mmHg PaO2 = 80 100 mmHg Mechanisms of Hypoxemia - Decreased inspired oxygen tension (FiO2) - Hypoventilation* - Ventilation Perfusion (V/Q) mismatching* - Shunt defect* - Diffusion defect *The more common causes of hypoxemia Normal Gas Exchange

Va = 5L/min

Q = 0L/min

Ventilation Diffusion

- Causes - Pulmonary embolism - Thrombus - Fat - Tumor Perfusion - Air - Septic - Pulmonary vasculitis

Diffusion Defect - Causes: - Acute Respiratory Distress Syndrome - Interstitial lung disease - Fibrotic lung disease Tracheobronchial Tree

Perfusion

Hypoventilation - Hypoventilation can also lead to decrese in arterial oxygen, even if theres no problem in parenchyma involved in gas exchange. Thus hypoxygenation can lead to hypoxemia.

Airways divide dichotomously Airway decreases in size surface area 70m2 80-120mL blood in capillaries for gas exchange

Va PAO2 PaO2 3

Diffusion Time Factors Affecting O2 Dissociation Curve

Carbon Dioxide Dissociation Curve

Extended Definition of Respiratory Failure Condition Ventilatory Failure Failure of arterial oxygenation Failure of O2 transport Definition Abnormality of CO2 elimination by the lungs Abnormality of O2 uptake by the lungs Limitation of O2 delivery to peripheral tissues so that aerobic metabolism cannot be maintained Inability of tissues to extract O2 from blood and use it for aerobic metabolism As PCO2 increases, oxygen carrying capacity diminishes. As PO2 increases (especially in venous blood) there is decrease in CO2 carrying capacity Bohr effect Oxygen Consumption O2 Consumption (VO2) VO2 = Q x (CaO2 CvO2) = 5 L/min x 5 mL/dL = 250 ml/min CvO2 oxygen content (venous) O2 Extraction ratio O2 ER = VO2 / DO2 = 250 mL/min / 1,000 mL/min = 0.25 (25%) Safety mechanism at subcellular level has good application for cardiac arrest must be able to resuscitate within 3-5 min still be able to avoid brain damage/death/organ failure Clinical Manifestations of Respiratory Failure - Apnea respiratory failure - Cyanosis 5 mg of desaturated Hb already; only 20% of patients with respiratory failure will present with cyanosis not a good parameter to measure - Altered level of consciousness - Dyspnea - Signs of respiratory distress - Signs/symptoms of hypoxemia - Signs/symptoms of hypercapnea - Signs/symptoms of underlying pathology Manifestations of Respiratory Distress and Respiratory Failure - Tachypnea and tachycardia - Flaring of ala nasae - Use of accessory muscles of respiration - Supraclavicular fossa excavation - Pump handle breathing - Tracheal tug and decreased tracheal length - External jugular venous distension in expiration - Costal paradox - Pulsus paradoxus - Abdominal paradox and asynchrony Respirator distress; but - Respiratory alternans there is impending - Cyanosis apnea ventilation - Altered level of consciousness failure in the next 15min Respiratory failure is not synonymous with respiratory distress. If theres respiratory distress, investigate if there is RF 4

Failure of O2 uptake and/or utilization

Oxygen Transport O2 transport (or delivery) (DO2) DO2 = Q x CaO2 = 5 L/min x 20 mL/dL x 10 = 1,000 ml/min Q cardiac output O2 content (CaO2) CaO2 = (1.39 x Hb x %Sat) + (0.003 x PaO2) = 1.39 x 15 x 0.98 + 0.003 x 98 = 20 ml/dl (vol%) Oxygenation Dissociation Curve

Note points PO2 = 40 mmHg g Saturation 75% (PvO2 for a normal person at rest) PO2 = 60 mmHg g Saturation 90% PO2 = 100 mmHg g Saturation 97.5% (PaO2 for a normal person at rest and in exercise) P50 = 26 mmHg g Saturation 50% (for normal Hb In sepsis, may have no hypoxemia, but hypoxia Hypoxemia <50 mmHg

Signs of Respiratory Distress - Tachypnea and tachycardia - Flaring of ala nasae - Use of accessory muscles of respiration - Intercostal muscle retraction - Sternocleidomastoid muscle contraction - Costal paradox (Hoovers sign) - Pump handle breathing - Supraclavicular fossae excavation - External jugular venous distension in expiration - Tracheal tug and decreased tracheal length - Abdominal paradox and asynchrony - Respiratory alternans Signs and Symptoms of Hypercapnea - Symptoms Headache Mild sedation Drowsiness Coma - Signs Vasodilation redness of skin, sclera and conjunctiva secondary to increased cutaneous blood flow; sweating Sympathetic response hypertension tachycardia Antok Signs and Symptoms of Hypoxia - Symptoms Ethanol-like symptoms confusion, loss of judgment, paranoia, restlessness, dizziness - Signs Sympathetic response tachycardia, mild hypertension, peripheral vasoconstriction Non-sympathetic response bradycardia, hypotension Lasing - Inhibitions depressed COPD chronic hypoxemia, irritable Diagnosis of Respiratory Failure - Patient is in respiratory distress - Hypoxemia (PaO2 < 60 mmHg) - Hypercapnia (PaCO2 > 50 mmHg) - Arterial pH shows significant acidemia (respiratory acidosis) *At least 2 of the 4 criteria should be fulfilled Only way to diagnose RF is to do ABG. It is a laboratory diagnosis, not a clinical diagnosis Other Diagnostic Modalities - Laboratory - CBC - Electrolytes - Imaging studies - Chest x-ray - CT scan - Ventilation-perfusion scan Evaluation of Causes of Hypercapnia Minute Ventilation (VE)

Evaluation of Hypoxemia - Normal P(A-a)O2 - Decreased FiO2 - Hypoventilation - Increased P(A-a)O2 - Ventilation-Perfusion mismatching - Shunt defect - Diffusion defect Most common cause of hypoxemia: hypoventilation, V/Q mismatch & shunt If with hypoxemia calculate first P(A-a)O2 gradient - Normal gradient no problem in respiratory membrane & V/Q, it will still go to arterial system Indices of Oxygenation Indices Normal Values 80 100 mmHg Pa O 2 Sa O 2 95 100 vol% 25 65 mmHg P(A-a)O2 PaO2/PAO2 0.75 350 450 PaO2/FiO2 <5% QS/QT PAO2 = (PB PH2O) x FiO2 (PaCO2/RQ) = (760 47) x FiO2 (PaCO2/RQ) = 713 x FiO2 (PaCO2/RQ) PaO2/PAO2 = 0.15 severe respiratory failure There are many oxygenation parameters. It is not adequate to look at just PaO2. Must look at other oxygenation parameters Algorithm of Hypoxemia P(A-a)O2

Normal

Increased

PaCO2

Challenge with 100% FiO2 Corrected PaO2 V/Q mismatch Shunt <10% Diffusion defect Uncorrected PaO2 Shunt >10%

Increased

Normal or Decreased Decreased FiO2

Hypo ventialtion

Principles of Treatment - Maintain adequate oxygenation - Support ventilation with mechanical ventilation when needed - Treat underlying illness or pathophysiologic derangements - Maintain fluid and electrolyte balance - Provide adequate nutrition - Avoid complications Decreased VE Transcribed by: Fred Monteverde Notes from: Cecile Ong Lecture recorded by: Lala Nieto Fred Monteverde Emy Onishi Cecile Ong Mitzel Mata Regina Luz Mae Olivarez Lala Nieto Chok Porciuncula Section C 2009!

Increased VE

Increased VCO2

Increased VD & Decreased VA

Decreased VA

Airway or Lung parenchyma disorders

Decreased ventilatory drive

Pump disorders

Fever Hypermetabolism

COPD, ARDS, Asthma, PE

Sedation Stroke

Neuromuscular disorder Pleural effusion